Using a sub-cutaneous and intracranial-orthotopic GBM model, we found that VDAC1 depletion resulted in inhibited tumor growth, with the residual tumor showing reversed oncogenic properties, including metabolic reprograming and inhibited proliferation, angiogenesis, EMT, invasiveness and stemness, leading to differentiation into neuron- and astrocyte-like cells 91 (Fig. 4). Here, VDAC1 is linked to glioblastoma.